Chronic obstructive pulmonary disease (COPD) is a serious progressive lung disease which makes it harder to breath. It currently affects over fifteen million people in the United States alone and is currently the third leading cause of death in the country. The overwhelming primary cause of COPD is inhalation of cigarette smoke, responsible for over 90% of COPD cases. The economic and social burden of the disease is both substantial and increasing.
FIG. 1 illustrates the anatomy of healthy lungs 100 including the trachea or wind pipe 102. As air flows in through the nose and mouth of an individual, the trachea 102 delivers the air to the lungs 100 for respiratory functions. The trachea 102 divides into the right main stem bronchus 104 and the left main stem bronchus 108. The right main stem bronchus 104 enters the right lung 106-1 and the left main stem bronchus 108 enters the left lung 106-2. In the lungs 100, both the right main stem bronchus 104 and the left main stem bronchus 108 divide into a plurality of bronchi 110, which further divide into a plurality of smaller airways referred to as bronchioles 112. Finally, these bronchioles 112 terminate into a plurality of alveoli 114. The alveoli 114 are small elastic air sacs which enable gas exchange. That is, they permit oxygen diffusion into the blood stream, and receive and expel CO2 during exhalation.
During inhalation, air is delivered to the lungs 100 and is received within the alveoli 114 via the bronchial passages or airways including the right and left main stem bronchi 104 and 108, bronchi 110, and bronchioles 112. The air inflates the alveoli 114, which later recoils to exhale air. This operation of lungs 100 during the inhalation and exhalation of air may be disturbed due to certain malfunctions or diseases, such as chronic obstructive pulmonary disease (COPD).
COPD includes both chronic bronchitis and emphysema. FIG. 2A illustrates a left lung 200 suffering from chronic bronchitis, which is shown in more detail in FIG. 2B. Chronic bronchitis is characterized by chronic cough with increased sputum, expelled mucus and saliva, production. Chronic bronchitis also causes airway inflammation 204, mucus hyper-secretion 206 that lines airway walls, airway hyper-responsiveness, and eventual fibrosis of the airway walls, which causes a serious limitation on airflow and gas exchange. The diameter of airways may also be reduced by one or more bronchoconstrictions 208, which constrict the airways in the lungs due to the tightening of surrounding smooth muscle. Airway restrictions may significantly increase the resistance to airflow through the airways, thereby preventing air from reaching or being expelled from alveoli 214. This resistance may be calculated according to Poiseulle's Equation (Equation 1) relating to laminar flow through a tubular member:
                    R        =                              8            ⁢                                                  ⁢            η            ⁢                                                  ⁢            l                                π            ⁢                                                  ⁢                          r              4                                                          (        1        )            Where:R=Resistance to flowη=viscosity of fluid (here, air)l=length of tube (i.e., airway)r=radius of the tube (i.e., airway)
Equation 1 indicates that the resistance to the flow of fluid, i.e., air, is proportional to the fourth power of the radius of the tube, i.e., airway. Thus, if the radius of the airway is reduced to half, the resistance to airflow in the lungs becomes 16 times the normal resistance. This increased resistance or limitation to airflow due to chronic bronchitis causes insufficient removal of carbon dioxide (CO2) from the lung 200, and manifests into hypercapnia (high blood gas levels of carbon dioxide). Hypercapnia leads to acidosis (lowering of blood pH levels), which correlates to a significantly greater risk of mortality.
There are thousands of small airways in the lungs and expanding or maintaining patency of these airways may facilitate better ventilation. However, due to the vast number of small airways, expansion or patency of these adversely affected airways may be very difficult. Moreover, breathing causes significant expansion and contraction of airways which may make deployment of rigid or semi-rigid airway support structures challenging and possibly impractical.
FIG. 3A illustrates a left lung 300 suffering from emphysema, which is shown in more detail in FIG. 3B. Emphysema is characterized by the destruction of the lung parenchyma, the functioning portions of the lung. The parenchyma includes alveoli walls, bronchioles, and bronchi. Destruction of the lung parenchyma may lead to loss of elastic recoil and tethering (i.e., ability to hold open walls of airways, including the bronchioles 112, leading to the alveoli 314 throughout much of inhalation and expiration), which maintains airway patency. Unlike larger lung airways, the bronchioles 112 are not supported by cartilage and thus have little intrinsic support. As a result, the bronchioles 112 are susceptible to collapse or reduce in diameter when destruction of tethering occurs, particularly during exhalation. A collapsed airway 304 is shown in FIG. 3B.
This loss in elastic recoil of an airway 304 leads to trapping of air and hyperinflation of the lungs, and also causes poor gas exchange. As a result, the alveoli 314 deteriorate into large, irregular pockets with gaping holes in their inner walls. This damages the alveoli 314 and reduces the surface area of the lungs and, in turn, the amount of oxygen that reaches an individual's blood stream.
Additionally, it may cause an increase in residual volume of the lungs, resulting in increased CO2 retention and reduced oxygen supply to the damaged alveoli 306. One existing approach to treat emphysema is performing lung volume reduction surgery, which removes or kills a portion of a diseased lung to allow greater expansion of remaining lung tissue. However, this approach is restricted to the upper portions (e.g., airways) of the lungs and poses a substantial risk of serious post-operative complications due to its invasive nature. Other existing approaches involve less-invasive techniques, including the use of endobronchial valves, reduction coils, heated water vapour, cryogenic therapy, and polymeric injections. However, the success of these approaches is heavily reliant upon the lack of collateral flow (shown in FIG. 4) between the targeted region of the lung and adjacent, non-targeted regions of the lung. For example, if an endobronchial valve or occlusion device 402 is implanted in a target airway 404 to prevent airflow into that region of the lung, if a collateral flow pathway 406 exists distal to the endobronchial valve 402, then airflow can still occur in the targeted region of the lung and atelectasis fails to fully occur. This limitation is common among a large portion of COPD patients.
Moreover, when a severe COPD patient is placed under exercise intensity, e.g., the patient is stressed due to exercise, dynamic hyperinflation occurs in the lungs due to which the patient is unable to expire quickly enough, causing further inflation of lungs with each successive breath. Additionally, the patient may suffer from dyspnea (i.e., significant shortness of breath), which deteriorates the patient's quality of life.
It may, therefore, be beneficial to provide a less-invasive technique of appropriately manipulating airways of the lungs for treating COPD, or other lung conditions.